Alzheimer’s

Disease
 What is Alzheimer’s Disease?

• It is the most common form of

dementia.
• Describe by a German physician,
Alois Alzheimer.
• Frau Auguste, first one diagnosed.
Dementia
 a syndrome of intellectual
deterioration severe enough to
interfere with occupational or
social performance.
 disturbances in memory, language
use, perception and motor skills,
and may interrupt the ability to
learn necessary skills, solve
problems, think abstractly and
make judgments.
 Anatomy of the Brain

Cerebrum - largest and uppermost

division of the brain.

contains Limbic System

contains frontal, parietal, temporal,
and occipital lobes.
Limbic System- “emotional brain”
– mediate emotions, learning
and memory
– consists of fornix, hippocampus,
cingulate gyrus, amygdala,
parahippocampal gyrus, and
parts of the thalamus.
Amygdala
• Limbic structure involved in many
brain functions, including
emotion, learning and memory.

Cingulate gyrus
• Plays a role in processing
conscious emotional experience.
Hippocampus
• Plays a significant role in the
formation of long- term memory.
Cortex
• Capable of storing and retrieving
both short and long-term memory.
 What is the Cause?

 There is no known
and proven to be
the primary cause
of AD but several
studies shows the
involvement of
plaques and
tangles in neurons.
1. Amyloid Plaques
 deposits of beta-amyloid protein that
accumulate in the spaces between
nerve cells.

Amyloid Beta protein

- protein fragments that the body
produces normally.
- a fragment of a larger protein called
Amyloid Precursor protein (APP).
2. Neurofibrillary Tangles

 deposits of protein tau that accumulate

inside of nerve cells.

Tau protein
- forms part of structure called
microtubules in the axon of neuron.
- protein that stabilizes the microtubules
when phosphorylated.
 Scientists are still studying how
plaques and tangles are related to
Alzheimer’s Disease. One theory
is that they block nerve cells
ability to communicate with each
other, making it difficult for
neurons to survive.
 Common Risk Factors

 Age
- The greatest known risk factor.
Most individuals with the illness
are 65 years and older.
 Genetic
- majority of AD cases are late-
onset and shows no inheritance.
However, in some families,
clusters of cases are seen.
- A gene Apolipoprotein E appears
to be a risk factor for the late-
onset of AD.
- Familial Alzheimer’s Disease or
earl y- on set disease is an
inherited rare form of the disease.
- It is cause by one of the gene
mutations on chromosome 1, 14,
and 21.
- mutation of APP gene on
chromosome 21.
 Symptoms and Stages

Cognitive Symptoms
2. Language difficulty
3. Memory loss
4. Poor judgement
5. Problems with abstract thinking
Behavioral Symptoms
2. Sleep disturbances
3. Hallucinations
4. Mood swings
5. Changes in personality
Stages of Al zheim er ’s Di sease

3. First Stage (mild)

• can last from 2 to 4 years
• Exhibit minor memory loss and
mood swings and are slow to
react and learn.
2. Second Stage (moderate)
• This is generally the longest stage
and can last 2 to 10 years.
• Can still perform task but needs
assistance with more complicated
activities.
• Clearly becoming disabled
3. Third Stage (severe)
• This stage may last 1 to 3 years.
• People may lose the ability to
feed themselves, speak,
recognize people, and control
bodily functions.
• Memory worsens
 DIAGNOSIS
 Diagnosis of Alzheimer’s Disease
are based on:
2. Mental and behavioral symptoms
3. Physical examination
4. Neuropsychological tests
 Mental and Behavioral
Symptoms
• Physician will normally take a
history of mental and behavioral
symptoms, using information
provided by patient and the
family.
 Physical Examination
• Physical examination will be
performed to help identify other
potential causes of dementia
• Includes blood tests, urinalysis,
etc.
• Magnetic Resonance Imaging
(MRI)
• Electroencephalogram
Neuropsychological Tests
• Identify behavioral and mental
symptoms associated with brain
injury or abnormal brain function

 Many scientists are searching

new ways to inexpensively and
reliably diagnose AD earlier and
with more accuracy.
 Treatments
• Common AD treatment
1) Acetylcholinesterase inhibitor
- Slow the metabolic breakdown of
acetylcholine and make more of
this chemical available for
communication between cells.
 *FDA APPROVED*
Brand Name Generic Name Side Effects Effective for
Nausea, vomiting,
1. Razadyne galantamine diarrhoea, weight loss Early to moderate AD
Nausea, vomiting,
diarrhoea, weight
2. Exelon rivastigmine loss, weakening Early to moderate AD
Nausea, vomiting, Early, moderate, and
3. Aricept donepezil diarrhoea, weight loss severe AD
Possible liver
damage, nausea,
4. Cognex tacrine diarrhoea Early to moderate AD
2) Glutamate Antagonists
– Namenda (memantine) is the only
currently available drug that adjust
the activity of glutamate
– Side effects are dizziness,
confusion, headache, and
constipation.
Parkinson’s
Disease
 What is Parkinson’s Disease?

 It is a degenerative disease of
CNS that often impairs the motor
skills and speech and other
functions.
 Named after James Parkinson, a
british physician who first
describe PD in his paper published
1817 about “Shaking Palsy”
 In our brain, the substantia
nigra which is a part of basal
ganglia have this
dopaminergic neurons that
produces dopamine.
 Dopamine is a
neurotransmitter responsible
for transmitting signals
between the sustantia nigra
and multiple brain regions.
 PD is characterized by
progressive destruction of the
nigrostriatal pathway, with
subsequent reduction in striatal
concentrations of dopamine.
 The mechanism by which the
brain cells in PD are lost may
consist of an abnormal
accumulation of the protein alpha-
synuclein.
 Alpha- synuclein
accumulation
forms
proteinaceous
cytoplasmic
inclusions called
Lewy Bodies.
While it is still not known what
causes PD, there are studies that
have found some environmental
and genetic link to the disease.
 Possible Causes
GENETIC
- Recent development in gene research
has found that genetic influence plays
a role in Parkinson’s Disease.

- 3 genes are identified that believed to

contribute to the disease. This include
alpha-synuclein, parkin, and ubiquitin
carboxyl- terminal hydrolase.
ALPHA- SYNUCLEIN GENE
• Located on chromosome 4
• Has been found to be associated
with dementia in PD patients.
• The mutations have also been
associated with the young onset
form of PD.
UBIQUITIN CARBOXYL-TERMINAL
HYDROLASE GENE
• Mutations in this gene have also
been found to cause abnormal
protein processing, where
proteins should be degraded.
When the gene is mutated,
abnormal processing results in
adverse cell reactions, which
eventually lead to cell death.
PARKIN GENE
• Parkin gene creates a protein also
called parkin, helps breakdown
defective proteins inside brain cells.
When the parkin gene is altered, this
function is impaired. It is hypothesized
that the accumulation of defective
proteins contributes to death of
neurons.
ENVIRONMENTAL

 TOXINS
• There are number of toxins that
can cause Parkinson symptoms in
humans.
• 1-methyl-4-phenyl-1,2,3,6-
tetrahydropyridine or MPTP, found
in some kinds of synthetic heroin.
Its toxicity possibly comes from
generation of reactive oxygen
species.
• Excessive accumulation of iron,
which are toxic to nerve cells.
Iron and other transition metal are
believed to bind to neuromelanin
in the affected neurons of the
substantia nigra. It generates
reactive oxygen species.
• Free radicals of mitochondria.
Free radicals are molecules that
damage membranes, proteins,
DNA. This damage is called
oxidative stress.
• Other suspected toxins are
pesticides, viruses and substance
that generates reactive oxygen
species.
HEAD TRAUMA
• Recent study found that those
who have experienced a head
injury are four times more likely to
develop PD than those who have
never suffered a head injury.
• Rare event, PD incidence is slight.
 Symptoms and Stages
 SYMPTOMS
Shaking (tremor) of the arms and
legs initially on one side of the body
while resting or walking.
Stiffness (rigidity) when an arm, leg,
or the neck is moved. The muscles
remain constantly tensed and
contracted, so the person feels stiff
and weak.
Slowness of movement
(bradykinesia), especially in starting
and attempting to continue rapid
repetitive movements.
Poor balance, difficulty walking with
shuffling of the feet.
Fatigue
Emotional changes such as
depression
Decline in mental function over time
Sleep disturbances
Problems with swallowing, speech,
bladder control and constipation
Small, cramped handwriting
Impaired sense of smell
Visual hallucinations
STAGES
Symptoms on one side of the body
only
Symptoms on both sides of the body.
No impairment of balance.
Balance impairment. Mild to
moderate disease. Physically
independent
Severe disability, but still able to
walk or stand unassisted.

Wheel chair- bound or bedridden

unless assisted.